Exam 2 lecture 5 Flashcards
steps for electrical conduction in heart
- SA node fires (pacemaker cells start beating)
- Excitation spreads through atrial myocardium
- AV node fire
- Excitation spreads down AV bundle
- Purkinje fibers distribute excitation through ventricular
PQRST meaning
P- beginning
Q- 1st dip
R- highest tip
S- Second dip
T- last beat
P wave is a culmination of
SA node, atrium and AV node
QT is determined by
Wide action potential mediated by Ca2+
What are some important ion channels in heart
Na channels
Calcium channels
K channels
HCN channels
hERG channels
What are the types of Na, Ca, K, HCN and hERG channels in heart
Na- Na V 1.5
Ca- N type, CaV 2.2, T type
K- Kir, Kv
HCN- HCN1, HCN 4
hERG- KCNH2, KV 11.1
what is an important channel to avoid targeting when developing new drugs
hERG
Membrane concentration of cells inside and outside of cells
inside
K- more K inside
Na- less Na inside
Ca- less Ca inside
Cl- less Cl inside
charge inside the cell vs outside the cell numerical value
inside- -70mV
outside- 0 mV
explain how an action potential is formed
-Na channels open and cause depolarization
-causes a rise in membrane potential
-Na channels close and there is a plateu when Ca cells come into cell and K cells go out of cell (cause contration)
- when Ca channel closes, rapid repolarization occurs
compare pacemaker cells and ventricular myocytes (important)
pacemaker cells
-specialized non-contractile cells
-physiologically depolarized
-Ca2+ dependent spikes
ACTION POTENTIAL -50mV
no plateu in image
Ventricular myocytes
- contractile cells
-hyperpolarized
-Na2+ dependent spikes
-86 mV action potential
long plateu phase
how does Ach affect Ca and HCN
reduce both
how does Ach affect ion channels
cause hyperpolarization and block activation of ion channels (reduce HR)
what are the 3 phases of Na channels in phase 0
Rest
open
inactivation
during rest- flat on graph
Open makes it shoot up
inactivation (ball and chain method ball plugs hole) causes a slow decline to rest)
can we form another action potential when channel is inactivated
no, it is called the refractory period
phase 2 and 3 of action potential generation
K+ channel opens and drives K out
Ca channel brings Ca inside
This causes a plateau
eventually ca channels will be inactivated then most of the force will be mediated by K channels, action potential goes down
Re entry arrhythmia requirements
- multiple parallel pathway
- Unidirectional block
- conduction time greater than ERP (effective refractory period)
What are the Antiarrhythmic drugs
Class 1- Na channel blockers
Class 2- B adrenergic antagonists
Class 3- K channel blockers (prolong refractory period)
Class 4 Caclium channel blockers
Which 2 classes of antiarrhythmic drugs have common features
Class 2 and 4 (B adrenergic and Ca2+)
Know the difference in how class 2 and class 4 look in EKG
Class 2 peaks have the same height
view notebook
CCB causes reduction in peak
How do B adrenergic agonists affect HR
slow it down
how do class 2 anti arrhythmics (BAR blockers) affect pacemakers? Ca currents? PR interval? refractoriness of AV node?
slow pacemakers
slow Ca currents
increase PR interval
increase refractoriness of AV node
are class IV anti arrythmics (CCBs) frequency dependent blocks
yes
How do class IV antiarrythmics affect refractoriness of AV node? PR interval? ventricular rate?
increase refractoriness of AV node
protects ventricular rate from tachycardia
